Sulforaphane-induced autophagy flux prevents prion protein-mediated neurotoxicity through AMPK pathway

• Published in: Neuroscience Vol. 278; pp. 31 - 39
• Main Authors: Lee, J.-H, Jeong, J.-K, Park, S.-Y
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 10.10.2014
• Subjects: AMP-Activated Protein Kinases - metabolism; AMPK; Apoptosis - drug effects; autophagy; Autophagy - drug effects; Autophagy-Related Protein 5; Cell Line, Tumor; Gene Knockdown Techniques; Humans; Isothiocyanates - administration & dosage; Microtubule-Associated Proteins - genetics; Neuroblastoma; Neurology; Neurons - drug effects; Neurons - metabolism; Neuroprotective Agents - administration & dosage; neurotoxicity; Peptide Fragments - toxicity; prion; Prions - toxicity; Signal Transduction - drug effects; sulforaphane; sulforaphane; RNA interference; autophagy-related 5; AMP-activated protein kinase; PrP Sc; LDH; mammalian target of rapamycin; TUNEL; neurotoxicity; propidium iodide; ethylenediaminetetraacetic acid; mTOR; prion; SFN; ATG5; prion protein; 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid; tuberous sclerosis complex1/2; scrapie prion protein; RNAi; autophagy; lactate dehydrogenase; terminal deoxynucleotidyl transferase dUTP nick end labeling; EDTA; PrP; HEPES; TSC1/2; AMPK; PI; PrPSc
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2014.07.072

Highlights • Sulforaphane protected neuron cells against PrP (106–126)-mediated neurotoxicity. • The protection effect of sulforaphane is induced through autophagy flux pathway. • The protection effect mediated by autophagy is regulated by AMPK signals.